Genetic structure in host species is often used to predict disease spread. However, host and pathogen genetic variation may be incongruent. Understanding landscape factors that have either concordant or divergent influence on host and pathogen genetic structuring is crucial for wildlife disease management. Devil facial tumor disease (DFTD) was first observed in 1996 and has spread throughout almost the entire Tasmanian devil geographic range, causing dramatic population declines. Whereas DFTD is predominantly spread via biting among adults, devils typically disperse as juveniles, which experience low DFTD prevalence. Thus, we predicted little association between devil and tumor population structure and that environmental factors influencing gene flow differ between devils and tumors. We employed a comparative landscape genetics framework to test the influence of environmental factors on patterns of isolation-by-resistance (IBR) and isolation-by-environment (IBE) in devils and DFTD. Although we found evidence for broad-scale co-structuring between devils and tumors, we found no relationship between host and tumor individual genetic distances. Further, the factors driving the spatial distribution of genetic variation differed for each. Devils exhibited a strong IBR pattern driven by major roads, with no evidence of IBE. By contrast, tumors showed little evidence for IBR and a weak IBE pattern with respect to elevation in one of two tumor clusters we identify herein. Our results warrant caution when inferring pathogen spread using host population genetic structure and suggest that reliance on environmental barriers to host connectivity may be ineffective for managing the spread of wildlife diseases. Our findings demonstrate the utility of comparative landscape genetics for identifying differential factors driving host dispersal and pathogen transmission.

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